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PhD opportunities at the Institute are typically open for applications between October and December of the year prior to the start of your studies.

Please find below the full list of projects on offer for the 2027 intake at the 99�Ⱦò������µ�ַ, follow the specific instructions on how to apply for each project in the advertisement, as the requirements of each differ.

Please do not send your application directly to the Institute, you must submit your applications through the University of Cambridge . Please see ''

For personal stories and tips on PhD studies from some of our researchers and to get a clearer view of the different roles available at the Institute, , read blogs by our students or visit our careers video page.

Here is the full list of PhD studentships on offer for the 2027 intake at the 99�Ⱦò������µ�ַ. 

The applications deadline for all PhD studentships: 8th December 2027
Please note interviews will be held the week commencing 18th January 2027

Bioscience South Cambridge doctoral training Partnership (BioSCaPe) is a transformative PhD programme designed to create the bioscience leaders of tomorrow.  Based in the heart of the world-leading Cambridgeshire bioscience cluster, BioSCaPe offers an unparalleled opportunity to combine cutting-edge research with entrepreneurial and leadership skills. BioSCaPe is a partnership between four world-leading research organisations; the 99�Ⱦò������µ�ַ, Wellcome Sanger Institute, MRC Laboratory of Molecular Biology, and the University of Cambridge in collaboration with major industry partners including AstraZeneca, Illumina, Alloy Therapeutics, and others, alongside the Babraham Research Campus and its network of bioscience companies.

Starting October 2027, 4-year Research Studentships will be available, leading to a University of Cambridge PhD degree, in the laboratories of Dr Jon Housley, Dr Teresa Rayon and Dr Arianne Richard at the 99�Ⱦò������µ�ַ.

Details of the 99�Ⱦò������µ�ַ’s interactive scientific programmes can be found on www.babraham.ac.uk. As a student at the Institute, you will have access to all of the outstanding science facilities, each one providing specialist equipment and expertise to support key research techniques and technologies. 
 
Project Title: The dark side of DNA
Project Outline
We think of DNA as a stable information source compartmentalised to the nucleus and mitochondria. When DNA enters the cytosol, it is recognised as a pathogen-associated molecular pattern by immune mechanisms that trigger inflammatory responses. However, a spectrum of diseases arise from mutations that increase formation or limit degradation of cytosolic DNA, even in the absence of infection. So, endogenous DNA must enter cytosol under normal conditions, but where this DNA comes from, why it is made and how it enters the cytosol remains largely mysterious. 
We have found that proliferating cells produce copious DNA that is exported from the nucleus, indicating that excess DNA synthesis is a normal, unavoidable part of nuclear metabolism. Many diseases including progerias (accelerated ageing conditions) are caused by mutations in DNA repair genes, while cytosolic chromatin is a characteristic feature of cellular senescence, raising questions as to whether DNA escaping the nucleus is a common factor in ageing and disease. 
We hypothesise that DNA egress from the nucleus is a major driver of disease and ageing, and is accentuated by mutations affecting DNA repair.
This PhD project will use bespoke DNA sequencing methods to quantify and profile populations of cytosolic DNA, investigate formation mechanisms, and reveal mechanistic links to ageing and disease.
Project Aims
1.    Refine methods to sequence cytosolic and secreted DNA in proliferating and quiescent cells carrying selected pathogenic mutations (WRN, ATM, ERCC1, RNASEH2, plus others that may be found to be relevant), then use DDR drugs to probe the DNA processing pathways generating this DNA.
2.    Apply these sequencing methods to tissue from young and old mice, to ask where cytosolic DNA accumulates and how this affects measured hallmarks of ageing. Once established, these methods could be applied to other tissues and/or clinical samples if available.
3.    Determine how different pathways of nuclear DNA egress lead to different immunogenic species, asking what is exported, where it goes, how it is processed and which immune receptors can be activated.
This project will involve a mixture of wet and dry lab techniques. The successful candidate will generate sequencing libraries and optimise methods, then perform their own bioinformatic analysis. When implementing novel sequencing pathways, it is critical that the bioinformatics is performed with a thorough understanding of the method. All necessary training will be provided but a keen interest in bioinformatics would be an advantage. The project will be carried out within the Epigenetics Programme at the 99�Ⱦò������µ�ַ, offering an outstanding interdisciplinary environment with expertise spanning epigenetics, development, signalling and ageing.
Principal Supervisor
Dr Jon Housley
Email address: jon.houseley@babraham.ac.uk 
Fully funded BioSCaPe iDLA Studentship
URL link to personal profile page or website: Jon Houseley » 99�Ⱦò������µ�ַ
Further details about the BioSCaPe iDLA including how to apply can be found here

Project Title:  Cross-Species determinants of stress susceptibility in PSC-derived Neural Progenitors and Spinal Motor Neurons
Life unfolds at remarkably different speeds across species, yet the molecular mechanisms that regulate developmental tempo remain poorly understood. A central unresolved question in developmental and evolutionary biology is how timing is controlled across species, with major implications for stem cell biology, regenerative medicine, and disease modelling. Emerging evidence suggests that stress responses, which vary across species and influence embryonic development, may act not only as protective mechanisms but also as active regulators of developmental timing and cellular maturation. However, it remains unknown how stress-response dynamics are integrated with developmental programs during neuronal differentiation, and how their dysregulation contributes to neurodevelopmental and neurodegenerative disease, including amyotrophic lateral sclerosis (ALS).
Motor neurons provide a powerful and clinically relevant system to address this question due to their high metabolic demand, intrinsic stress sensitivity, and selective vulnerability in ALS and related disorders. Pluripotent stem cell (PSC)-derived motor neurons are widely used for disease modelling and neurotoxicity screening, but show substantial variability across species and developmental states. Whether this reflects developmental maturity, species-specific biology, or intrinsic differences in stress responsiveness remains unresolved.
Building on previous work demonstrating conserved differences in motor neuron developmental tempo between mouse and human (Rayon et al., Science, 2020; Nakanoh, Stamataki et al., bioRxiv, 2025), this four-year industrial PhD project, in partnership with Axol, will establish a cross-species and disease-relevant stem cell platform to define how developmental state and species identity shape neuronal stress susceptibility, with direct relevance to ALS.
Using pluripotent stem cell (PSC)-derived neural progenitor cells (NPCs) and spinal motor neurons (MNs) from multiple mammalian species, the student will investigate how stress responses emerge during neuronal differentiation and how they relate to developmental tempo, maturation, and disease-relevant vulnerability.
Project aims:
1.    Develop a harmonised cross-species stem cell platform by generating spinal motor neurons from multiple mammalian PSC lines, including human and non-human primates.
2.    Define how stress susceptibility changes during neuronal development by comparing neural progenitor cells and motor neurons.
3.    Identify molecular signatures of stress resilience and vulnerability using comparative proteomic profiling.
4.    Determine how stress-response pathways influence developmental timing and neuronal maturation through targeted functional perturbations.
Overall, this four-year industrial PhD project will uncover how stress biology is integrated into neural developmental programs across species, and how this integration shapes motor neuron maturation, resilience, and vulnerability in ALS.
Research environment
The Rayon Lab investigates the molecular and metabolic mechanisms that regulate biological timing, developmental tempo, and lifespan across species. The group combines stem cell and embryo models with quantitative experimental and computational approaches to understand how developmental processes evolve and are regulated.
The project is based at the 99�Ⱦò������µ�ַ and will be conducted in close collaboration with Axol, providing exposure to both academic and industrial research environments. The student will have access to state-of-the-art facilities and expertise in stem cell biology, developmental biology, imaging, genomics, proteomics, and computational analysis.
Candidate profile
We welcome applications from motivated students with interests in developmental biology, stem cells, neuroscience, evolution, or quantitative biology. Previous experience in cell culture, molecular biology, bioinformatics, or programming would be advantageous but is not essential, as full training will be provided.
This project offers a unique opportunity to address a fundamental biological question while developing innovative stem cell technologies with direct relevance to disease modelling, drug discovery, neurotoxicity testing, and the development of more predictive preclinical models. Informal enquiries, including a brief statement of motivation, are encouraged. Please contact Teresa Rayon.
Principal Supervisor
Dr Teresa Rayon
Email address: Teresa.rayon@babraham.ac.uk  
Fully funded BioSCaPe iDLA Studentship
URL link to personal profile page or website: Teresa Rayon | 99�Ⱦò������µ�ַ
Further details about the BioSCaPe iDLA including how to apply can be found here

Project Title: T cell signalling in fibrotic feedback loops
Fibrosis is a pathological feature of many chronic inflammatory diseases, characterized by extracellular matrix (ECM) dysregulation, connective tissue accumulation, and complex immune-stromal feedback loops. Studies of cytotoxic (CD8) T cells in fibrotic tissues have revealed altered phenotypes and suppressed function, and there is evidence to suggest that while functional CD8 T cells can prevent or resolve fibrosis, their dysregulation in the fibrotic environment contributes to tissue decline. We are interested in the signalling mechanisms underlying the fibrosis-associated T cell state, specifically in the context of endometrial fibrosis. 
Endometriosis is a debilitating condition affecting 10% of women of child-bearing age that has no cure. The fibrotic tissue environment is a key feature of endometriosis and is characterized by particularly high levels of TGF and dysregulated IL-15, which are known to regulate differentiation state, cytotoxic function, and both antigen-driven and antigen-independent activation of CD8 T cells. This project will examine the endometriosis-associated cytokine milieu, signalling of these cytokines in CD8 T cells, and the molecular mechanisms connecting this signalling to altered differentiation state and function.
The project is a collaboration between the Richard Lab at the 99�Ⱦò������µ�ַ and Cyclana Bio. The Richard Lab studies how T cell activity is altered by variations in antigen binding and the microenvironment 1-4. Cyclana Bio is a biotech company with a mission to develop disease-reversing therapeutics to cure endometriosis. Cyclana also has strong academic roots in ECM biology 5. The project will leverage the T cell expertise and experimental platforms from the Richard lab alongside endometriosis expertise and novel 3D tissue models developed by Cyclana Bio to examine the consequences of fibrosis-associated cytokine signalling in CD8 T cells. We are particularly focused on gaining mechanistic insight by identifying signalling, epigenetic, transcriptomic, and/or translational mediators of differentiation and functional effects.
The student will have the opportunity to work in both industry and academic settings. They will be involved in all aspects of project planning, experimentation and analysis, with support from other team members. At Cyclana, the student will experience a small biotech working environment, contribute to work with clinical samples, and learn to use 3D tissue models with advanced tissue culture and imaging techniques. At the 99�Ⱦò������µ�ַ, the student will benefit from a highly collaborative institute with collective expertise in Immunology, Signalling, and Epigenetics, and will have the opportunity learn a variety of immunological and genomic techniques including functional secretion and cytotoxicity assays, migration assays, signalling measurements, flow cytometry, single-cell and bulk transcriptomics, proteomics, CUT&Tag, CRISPR/Cas9 genome editing, and bioinformatic and statistical analysis of generated data. The student will share their research through publications and presentations at internal meetings and external conferences in both academic and industrial settings.
References
1.    Panova V, et al. T cell receptor-ligand affinity quantitatively tunes transcriptome remodelling in vivo, inversely regulating cell division and interferon response (2026) BioRxiv.
2.    Richard AC. Divide and conquer: phenotypic and temporal heterogeneity within CD8+ T cell responses. (2022) Front Immunol, 13:949423.
3.    Ma CY, et al. Stimulation strength controls the rate of initiation but not the molecular organisation of TCR-induced signalling. (2020) Elife, 9:e53948.
4.    Richard AC, et al. T cell cytolytic capacity is independent of initial stimulation strength. (2018) Nat Immunol, 19(8):849–58.
5.    Mui BWH, Hyaluronic acid and tissue mechanics orchestrate mammalian digit tip regeneration. Science (2026) 392(6794):eady3136.

Principal Supervisor
Dr Arianne Richard
Email address: Arianne.Richard@babraham.ac.uk 
Fully funded BioSCaPe iDLA Studentship
URL link to personal profile page or website: Arianne Richard | 99�Ⱦò������µ�ַ
Further details about the BioSCaPe iDLA including how to apply can be found here

The Cambridge Biosciences Doctoral Training Partnership (DTP), funded by the Doctoral Landscape Awards under UKRI. brings together four world-leading research institutions — the University of Cambridge, the 99�Ⱦò������µ�ַ, the National Institute of Agricultural Botany (NIAB), and the Wellcome Sanger Institute — in partnership with UK Research and Innovation (BBSRC).
It aims to train the next generation of Bioscience leaders by providing research projects in our world leading groups, complemented by a training and cohort-building programme to develop their professional and transferable skills, and opportunities to work in diverse professional environments.
This programme provides training opportunities across the scientific areas encompassed by the Biotechnology and Biological Sciences Research Council (BBSRC) strategic research priorities:
•    Understanding the rules of life
•    Transformative technologies
•    Bioscience for sustainable agriculture and food
•    Bioscience for renewable resources and clean growth
•    Bioscience for an integrated understanding of health.
Further information about the Cambridge Biosciences DTP PhD Programme can be found here.
Starting October 2027, a 4-year Targeted Research Studentship will be available, leading to a University of Cambridge PhD degree, in the laboratory of Dr Philipp Voigt at the 99�Ⱦò������µ�ַ.
Project title: Poised Chromatin and the Epigenetic Control of Development
Project outline
How cells switch genes on and off at the right time is fundamental to development. In embryonic stem cells, many genes whose expression is required later in development are kept in a ""poised"" state, ready to be activated during cell lineage commitment. This poised state is controlled by chromatin, where specific histone marks create regulatory environments that either promote or repress gene expression. However, the mechanisms that allow these poised genes to respond rapidly to developmental signals remain poorly understood.
Our recent work has identified several previously uncharacterised histone acetylation marks at these poised genomic regions, known as bivalent chromatin domains. This project will investigate how these acetylation marks control gene expression during cell differentiation and development.
The student will test whether the acetylation marks recruit specific ""reader"" proteins that help activate developmental genes or influence gene repression pathways. Using embryonic stem cell models, the project will examine where these proteins bind across the genome, how they are recruited to chromatin, and how they affect gene activity as cells differentiate. The student will also identify additional factors that work together with these proteins to regulate developmental gene expression.
The project combines molecular biology, genomics, biochemistry and stem cell biology. Training will include genome-wide approaches such as ChIP-seq and RNA-seq, bioinformatic data analysis, CRISPR-based genome editing, stem cell differentiation, protein degradation systems, chromatin biochemistry and proteomics. The work will provide broad training in epigenetics and gene regulation while addressing a fundamental question in developmental biology.
The project will be carried out within the Epigenetics Programme at the 99�Ⱦò������µ�ַ, offering an outstanding interdisciplinary environment with expertise spanning epigenetics, development, signalling and ageing.
Principal Supervisor
Dr Philipp Voigt
Email address: philipp.voigt@babraham.ac.uk 
Fully funded Cambridge Biosciences Doctoral Training Partnership (DTP) Targeted Studentship (Project Reference: TRG27-BAB-PV1)
URL link to personal profile page or website: Philipp Voigt | 99�Ⱦò������µ�ַ
Further details about the Cambridge Biosciences Doctoral Training Partnership (DTP) including how to apply can be found here.
 
PhD in Biological Science (99�Ⱦò������µ�ַ). The 99�Ⱦò������µ�ַ is a world-leader in fundamental biological research investigating the systems that underpin development and healthy ageing. We support full-time PhD students on three-to-four-year studentships and the projects mentioned below are open for applications. Please note, these studentships are competition funded studentships (unfunded) and so you will need to apply for your own funding. Possible sources of funding include the University of Cambridge-wide funding competitions, such as the Gates Cambridge Trust and Cambridge Trust (please visit the University of Cambridge Funding Search webpage). Please ensure you check the postgraduate funding competition box when applying.

Project Title:  Spatial Control of Wnt–ERK Signalling by Glypican-Dependent Ligand Dispersal in Development and Disease
Glypicans are a family of heparan sulfate proteoglycans that regulate extracellular signalling environments during development. Human genetics highlights the importance of this regulation: loss-of-function mutations in GPC6 cause omodysplasia, a rare skeletal dysplasia characterised by impaired growth and developmental defects. More recently, genetic studies have implicated glypicans in neurological disease, with emerging links to disorders including schizophrenia and Parkinson’s disease. Despite these associations, the molecular mechanisms by which glypicans shape signalling outputs in different tissues remain poorly understood.
Recent work has identified a conserved role for GPC6 in controlling the extracellular distribution of Wnt ligands. Disruption of this process collapses Wnt gradients and leads to spatially restricted signalling, suggesting that glypicans regulate not only the range but also the intensity of morphogen signalling. We have found that loss of GPC6 function leads to hyperactivation of ERK signalling, through dysregulated non-canonical Wnt pathway activity. This suggests that extracellular control of Wnt ligand distribution can directly influence intracellular signalling output, but the molecular mechanisms linking these processes remain unclear.
This project will investigate how glypican-dependent regulation of Wnt signalling is coupled to ERK activation, with a particular focus on identifying the signalling cascade linking extracellular ligand organisation to downstream pathway output. Particular emphasis will be placed on the role of small GTPase-mediated signalling in integrating spatially restricted Wnt signals and modulating intracellular pathway activity.
The project will primarily focus on the nervous system, where non-canonical Wnt signalling plays key roles in regulating cell polarity, migration, neurite outgrowth, and neuronal specification. These processes are essential for the formation and maintenance of neural circuits and have been increasingly implicated in neurodevelopmental and neurodegenerative disorders. The student will investigate whether loss of GPC6 leads to dysregulated Wnt–ERK signalling in the developing mouse brain, with a particular focus on dopaminergic neuron specification and patterning.
To explore relevance to human disease, the project will use induced pluripotent stem cell (iPSC)-derived neurons and astrocytes to test whether similar signalling mechanisms operate in human cells. A key aspect of the project will be to define the downstream consequences of dysregulated Wnt–ERK signalling in neural cells. Non-canonical Wnt signalling, including Wnt5a-dependent pathways, plays an important role in neuronal maturation, regulating cytoskeletal organisation, neurite development, and synaptic connectivity—processes that intersect with ERK-dependent signalling networks. The student will investigate how perturbation of GPC6 alters these downstream responses, with a particular focus on identifying signalling targets and cellular behaviours that are Wnt-Erk regulated. Understanding these outputs will be important not only for defining core biological mechanisms, but also for improving in vitro models of neuronal differentiation and maturation, ensuring that iPSC-derived neurons faithfully recapitulate relevant developmental signalling states.
Together, this project will define how extracellular regulation of morphogen signalling is translated into intracellular pathway activation, providing new mechanistic insight into how disruption of signalling architecture can contribute to developmental defects and neurological disease.
This project will be undertaken with BitBio.
Principal Supervisor
Dr Ian McGough
Email address: Ian.McGough@babraham.ac.uk 
Competition funded studentship (unfunded) – You will need to apply for your own funding, possible sources of funding include the University of Cambridge-wide funding competitions, such as the Gates Cambridge Trust and Cambridge Trust (please visit the University of Cambridge Funding Search webpage). Please ensure you check the postgraduate funding competition box when applying.
URL link to personal profile page or website: Ian McGough | 99�Ⱦò������µ�ַ

Project Title: Fantastic proteins and where to find them: exploring the biology of histones outside the nucleus
Histone proteins package DNA within the confines of the nucleus in a macromolecular structure called chromatin. They additionally modulate the accessibility of DNA to gene and epigenetic regulators through the chemical modifications they carry (post-translational modifications, PTMs). Beyond their fundamental functions in genome packaging and regulation, histones have a life outside the nucleus: they are potent antimicrobial agents and the externalization of chromatin as an immune defense mechanism is a process that is as ancient and widespread across three of life as chromatin itself 1,2. We have discovered that histones are externalized in previously unappreciated contexts, beyond immune cells and immune defense. This discovery opens a new frontier in cell biology and the study of chromatin.
Our lab focusses on the study of histone citrullination3, the only known PTM specifically associated with histone externalization – indeed, extracellular histones are practically impossible to detect with confidence using current analytical methods, but citrullination can be used as a beacon that helps us locate this particular histone pool. Using tools and systems we have developed for the study of citrullination4-8, we are well placed to investigate the biology of extracellular histones in a variety of physiological or pathophysiological contexts. 
This project will investigate the biology of histone externalization during tissue development, homeostasis and ageing. The work will be organized in three specific aims, which will address the following questions:
1) What is the mechanism of tissue externalization?
We will employ cell biological and biochemical analyses, coupled with powerful imaging technologies, to understand the pathways through which citrullination is activated and histones are externalized.
2) What are the consequences of extracellular histone sensing by neighbouring cells?
We will employ protein biochemistry and genome sequencing technologies to understand the signalling, transcriptomic and epigenetic changes undergone by cells that come in contact with extracellular histones. Our findings so far indicate that these cell responses differ drastically depending the age of the recipient cells, thus this aim will allow us to investigate how cell resilience is eroded during ageing.
3) Which molecular pathways mediate the responses to extracellular histone?
Using the readouts identified in Aim 2 and high-resolution proteomic analyses, we will aim to identify the molecules that mediate extracellular histone responses. 
Through this research we will investigate a novel type of cell communication and its roles in mammalian development and ageing. The student who undertakes this work will obtain training in cell and developmental biology, protein biochemistry, genomics, proteomics, state-of-the-art imaging and bioinformatic analyses.  Although we have a particular interest in developmental biology, tissue stem cells and ageing, the student joining our lab will have the opportunity to incorporate their own interests and inform the direction of their project. 
References:
1.    Sollberger G., Tilley D.O., Zychlinsky A. (2018). Neutrophil Extracellular Traps: The biology of chromatin externalization. Dev Cell 44(5):542-553. doi: 10.1016/j.devcel.2018.01.019. PMID: 29533770.
2.    Grinat J., Shriever, N.P., Christophorou M.A. (2024). Fantastic proteins and where to find them – histones, in the nucleus and beyond. J Cell Sci, 137(24):jcs262071. doi: 10.1242/jcs.262071. PMID: 39704565.
3.    Christophorou M.A. (2022). The virtues and vices of protein citrullination. R Soc Open Sci. 9(6):220125. doi: 10.1098/rsos.220125. PMID: 35706669.
4.    Christophorou, M.A.*, Castelo-Branco, G.*, Halley-Stott, R., Slade Oliveira C., Loos R., Radzisheuskaya A., Mowen K., Bertone P., SIlva J.C.R., Zernicka-Goetz M., Nielsen M.L., Gurdon J.B., Kouzarides T. (2014). Citrullination regulates pluripotency and histone H1 binding to chromatin. Nature 507:104–108. doi: 10.1038/nature12942. PMID: 24463520.
5.    Cummings T.F.M., Gori K., Sanchez-Pulido L., Gavriilidis G., Moi D., Wilson A.R., Murchison E., Dessimoz C., Ponting C.P., Christophorou M.A. (2022). Citrullination Was Introduced into Animals by Horizontal Gene Transfer from Cyanobacteria. Mol Biol Evol. 39(2):msab317. doi: 10.1093/molbev/msab317. PMID: 34730808.
6.    Singh A., Khan S., Moore D., Andrews S., Christophorou M.A. (2023). Transcriptomic analysis of PADI4 target genes during multi-lineage differentiation of embryonic stem cells. Philos Trans R Soc Lond B Biol Sci, 378(1890): 20220236. doi: 10.1098/rstb.2022.0236. PMID: 37778387.
7.    Bertran M.T.*, Walmsley R.*, Cummings T., Aramburu I.V., Benton D.J., Mora Molina R., Assalaarachchi J., Chasampalioti M., Swanton T., Joshi D., Federico S., Okkenhaug H., Yu L., Oxley D., Walker S., Papayannopoulos V., Suga H., Christophorou M.A.**, Walport L.J.** (2024). A cyclic peptide toolkit reveals mechanistic principles of peptidylarginine deiminase IV regulation. Nat Commun. 15(1):9746. doi: 10.1038/s41467-024-53554-1. PMID: 39528459;.
8.    Rebak A.S., Hendriks I.A., Elsborg J.D., Buch-Larsen S.C., Nielsen C.H., Terslev L., Kirsch R., Damgaard D., Doncheva N.T., Lennartsson C., Rykær M., Jensen L.J., Christophorou M.A., Nielsen M.L. (2024). A quantitative and site-specific atlas of the citrullinome reveals widespread existence of citrullination and insights into PADI4 substrates. Nat Struct Mol Biol. 31(6):977-995. doi: 10.1038/s41594-024-01214-9. PMID: 38321148.

Principal Supervisor
Dr Maria Christophorou
Email address: Maria.Christophorou@babraham.ac.uk 
Competition funded studentship (unfunded) – You will need to apply for your own funding, possible sources of funding include the University of Cambridge-wide funding competitions, such as the Gates Cambridge Trust and Cambridge Trust (please visit the University of Cambridge Funding Search webpage). Please ensure you check the postgraduate funding competition box when applying.
URL link to personal profile page or website: Maria Christophorou | 99�Ⱦò������µ�ַ